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Acute Mountain Sickness

000 ft (3.000 m)  Ozone layer starts .000 m)  life is endangered without supplemental oxygen •From 40.PHYSIOLOGICA LY CRITICAL ALTITUDES: •Up to 10.000 m)”safe zone of rapid ascent”classically defines ‘high altitude’ •At 18.500 m)  upper limit of permanent human inhabitation •Above 20.000 ft(12.000 ft (5.000 ft (6.

e.000) 70 HbSATURATI ON in % ~ 97 % ~ 90 % ~ 80 % < 70 % EFFECTS Stages (if any) NIL Usually none.500 – 6.sealevel) 160 Upto 10.Mental and muscle fatigue Severe hypoxic symp  aggravated CNS involvement Seizures and muscle twitching .000 (3.000 (4.500) 98 15.000 – 15.000 – 4.000) 110 10. COMMON HYPOXIC EFFECTS WITH DIFFERENT ALTITUDES: ALTITUD INSPIRE E LEVEL D AIR PO2 In feet (metre) In mm of Hg 0 (i. +/.000 – 20.000 (3.some nocturnal visual reduction ( of indifference) Mod. Hypoxic symptoms Drowsiness. headaches .

PHYSIOLOGICAL RESPONSES TO HIGH ALTITUDE HYPOXIA: I) Acute responses Refers to immediate reflex adjustments of respiratory and cardiovascular system to hypoxia II) Long term responses (acclimatization) Refers to changes in body tissues in response to long term exposure to hypoxia .

ACCOMMODATION AT HIGH ALTITUDE:  Respons akut tubuh saat terjadi hipoksia : Hyperventilation: arterial PO2   stimulasi kemoreseptor perifer  meningkatkan ventilasi. . Tachycardia: O2 jaringan   Respons   frekuensi jantung  distribusi oksigen ke jaringan.

lack of coordination.Neurological : • Considered as “warning signs” • Depression of CNS  feels lazy. headache • ‘Release Phenomena’ like effect of alcohol. convulsion & finally . slurred speech. sleepy. twitching. slowed reflexes. overconfidence • At further height  cognitive impairment. poor judgment.

who ascends to very high altitudes over 1-2 days for first time.Acute Mountain Sickness • Bisa terjadi pada ketinggian diatas 1500 m (4920 ft) umumnya pada ketinggian 2500 m. • No predeliction based on gender • More likely if : –Rapid ascent –Lack of acclimatization . • Symptom-complex occurring in a lowlander.

000 feet : 75 %  Report from Colorado ski resort : 12 %  Can occur in those with no prior problems with altitude exposure  Can recur (no consistent tolerance or "immunity") .000 feet (3000 meters) : 30 %  Sudden ascent > 14.insidensi  Sudden ascent > 10.

with Cerebral oedema (↓pO2  arteriolar dilatation limit of cerebral autoregulatory mechs are crossed  ↑cap.pressure ↑fluid transudation into brain tissue) or Alkalosis In the minority.•Acute Mountain Sickness: •Cause exactly not known appears to be assoc. more serious sequelae – highaltitude pulmonary oedema and high-altitude cerebral oedema develop. .

Adaptive mechanisms • As PaO2 declines to 60mmHg chemosensors in the carotid body trigger an increase in minute ventilation: Hypoxic Ventilatory vesponse (HVR) • PCO2 drops --> resp alkalosis --> limits HVR. Himalayan Peaks over Kathmandu. Nepal .

(Lundby . • 4-5days: hematopeisis Himalayan Peaks Nepal afterover 4-5Kathmandu. • Catecholmine release --> increase in HR and PAP. • Increase in cerebral blood flow: offset by the vaso-constrictive effect of hypocapnea. Acclimatization correlates with return of resting HR to baseline except at extreme altitude. days.Adaptive mechanisms • 24-48h: bicarbonate diuresis --> compensatory metabolic acidosis --> minute ventilation increases.

Gejala • Gejala terjadi pada 8-24 jam setelah tiba. nausea or vomiting – Fatigue or weakness – Dizziness or lightheadedness – Difficulty sleeping . dapat berlangsung selama 4-8 hari. • Gejala khas : HEADACHE disertai one or more symptom: – Anorexia.

excretion through kidneys)  If remain untreated . it may cause— Ataxia. Disorientation.coma & Finally Death(d/t tentorial herniation of the brain-tissue) . Symptoms can be reduced by— • ↓Cerebral oedema by large doses of Glucocorticoids • ↓Alkalosis by Acetazolamide (inhibits CA↓H+ & ↑HCO3.

AMS .Pathophysiology .